Cervical artery strokes -
Serious complications with neck manipulation and informed consent
LESSONS FROM PRACTICE
MJA 21st August 2000
Vol 173, Number 4 p213
Serious complications with neck manipulation and informed consent
Patient 1
A 27-year-old woman had chiropractic manipulation for right shoulder
stiffness. She had previously been well, with no history of diabetes,
hypertension or neck trauma. She had four neck manipulations within one
month; the first three were uneventful and provided some pain relief. Within
48 hours of the fourth manipulation, she developed right facial, trunk and
limb paraesthesiae with mild dysphagia. She had no headache, vertigo or
ataxia. Computed tomography (CT) scans of head and cervical spine were
normal, except for mild misalignment of the C5 vertebra. Her general
practitioner advised conservative management.
Symptoms fluctuated during the following five months before worsening right
facial paraesthesiae led her to seek specialist
advice. She denied pain or distress and was apyrexic, with a pulse rate of
80 bpm and blood pressure of 130/80 mmHg. There were no heart murmurs or
bruits. Pupils were equal
and reactive, with normal fundi, She had mild right facial asymmetry but no
other neurological signs. Vertebral artery dissection (VAD) was suspected.
A magnetic resonance imaging (MRI) scan with angiography revealed complete
termination of flow in the distal portion of the right vertebral artery (VA)
at about the level of the C3/C4 intervertebral disc space (Figure 1). Axial
scans showed high signal strength in the region of the VA lumen consistent
with thrombus through this segment, with minimal to no patency. Collateral
vessels, with some refilling of the right VA more distally, suggested
chronic dissection. No intracranial
infarct was seen.
The patient was placed on aspirin, and had only minimal right facial
paraesthesiae on follow-up at one month.
Patient 2
A 37-year-old man sought chiropractic treatment for a persistent bitemporal
headache of four weeks' duration. On history, the headache seemed to be of
muscular tension type. The patient had previously been well, with no history
hypertension, diabetes or neck trauma. He smoked 20 cigarettes daily, drank
little alcohol, took no regular medications, and had no relevant family
history. Immediate following his first cervical manipulation, while still in
the chiropractor's rooms, he reported severe diplopia, dysarthria and
ataxia. He sat in the waiting room for an hour before driving back to his
office; he was not advised to seek a medical opinion. The symptoms worsened,
and a colleague drove him home, where he slept. On waking, he had only mild
headache.
Two days later, the patient presented to hospital with severe ataxia, nausea
and vomiting, and complaining of vertigo, diplopia and right-sided neck
pain. He was afebrile had a pulse rate of 88 bpm and a blood pressure of
130/80 mmHg. He had no heart bruits or murmurs, and was alert and oriented.
His pupils were equal and reactive, with normal fundi. Nystagmus and
diplopia were present bilaterally, but more pronounced on right gaze. He had
a profound right sensorineural hearing loss (confirmed by audiometry). The
other cranial nerves were normal. Ataxia was predominantly right-sided, with
upper-limb past pointing, intention tremor, poor heel-shin coordination,
'ataxic wide-based gait, and a tendency to fall to the right. Tone and power
were essentially normal bilaterally, with symmetrical deep tendon reflexes
and downgoing plantar
responses. Dissection of vertebral artery with emboli was suspected.
Cerebral CT scan suggested a right brainstem infarct, and the patient was
commenced on intravenous heparin. Routine blood tests, electrocardiogram and
chest films were unremarkable (apart from a cholesterol level of 6.0 mmol/L
[normal range, 3.9-5.5 mmol/L] and triglyceride level of 2.79 mmol/L [normal
range, 0.5-1.7 mmol/LI). An MR1 scan five days after presentation showed
multiple infarcts within the deep white matter of both cerebellar
hemispheres, and a well defined, wedge-shaped infarct of the inferior aspect
of the right cerebellar hemisphere, with involvement of the adjacent portion
of the right middle cerebellar peduncle without appreciable mass effect
(Figure 2). Axial scans demonstrated high signal strength in the vessel wall
consistent with mural thrombus. Magnetic resonance angiography demonstrated
a patent right VA, but there was minimal to no filling of the left VA for
virtually its entire extracranial course (Figure 3). Appearances were
consistent with a left VAD, a large right anterior inferior cerebellar
artery territory infarct, and several smaller infarcts in the superior
cerebellar artery territory.
The symptoms of vertigo, nausea and vomiting settled quickly, with residual
diplopia, hearing impairment and rightsided limb and gait ataxia. Following
initial physiotherapy, occupational therapy and alternate eye patching, the
patient was transferred for rehabilitation. At outpatient review one month
later, he was mildly ataxic, with right-sided past pointing and intention
tremor. During the following six months, his symptoms resolved further but
the diplopia and ataxia failed to resolve.
(Discussion)
VERTEBRAL ARTERY DISSECTION (VAD) is the most common cause of posterior
circulation infarction in young people.' It remains the leading cause of
cerebellar infarction' and can be responsible for considerable morbidity, as
seen with Patient 2, who has residual ataxia, diplopia and sensorineural
deafness. Extracranial dissections are more commonly trauma related, whereas
intracranial dissections are usually spontaneous2,3. There are no proven
methods of risk reduction for spontaneous VAD.
Cervical manipulation is often perceived as benign and risk-free4. However,
postmortem studies6 support the belief that rotary head movements and
hyperextension of the neck, such as those used in chiropractic neck
manipulation4 and presumably used in both of our patients, may narrow
arterial lumens and cause kinking. Case reports have related the onset of
posterior circulation symptoms to cervical manipulation in the absence of
another explanatory event5. An increased awareness of this relationship
might prompt earlier investigations Looking for VAD.
The exact incidence of VAD following cervical manipulation is unknown5, and
its determination may be complicated by the occurrence of asymptomatic
dissections2,3 and by the possibility of significant delays before a
symptomatic event, whether it be due to embolism or progression of the
dissection to complete occlusion of
the artery.2,5
The association of neck manipulation and VAD, with the potential for
subsequent stroke, has been well established 1,2,5 yet in neither patient
was this discussed with the patient before they "consented" to undergo the
procedure.
Chiropractors are not the only therapists who perform neck manipulation.
Physiotherapists, some occupational therapists, orthopaedic surgeons, family
physicians dealing in manipulative management, and even some neurologists,
offer various types of physical manipulative intervention. We suspect that
they too neglect to warn patients of the very real potential for serious
adverse effects from this type of treatment.
Any procedure which carries a significant material risk to the patient must
be performed only if the therapist has gained informed consent7. Many
manipulative procedures are performed for relatively minor complaints4, and
may lack proven potential for benefit. Patients must be in a position to
decide whether they are prepared to accept the risks associated with these
procedures.
Information on the risks and the lack of proven benefit should be routinely
relayed to the patient, not only to gain informed consent, but also to
encourage the patient to seek prompt attention should he or she experience
any symptoms suggestive of VAD.
Roy G Beran,* Andrew Schaefert Toos Sachinwalia*
*Senior Visiting Medical Officer, Department of Neurology
t Neurology Registrar, Department of Neurology t Neuroradiologist,
Department of Radiology Liverpool Hospital, Sydney, NSW
1. Barinagarrementeria F, Amaya LE, Cantu C. Causes and mechanisms of
cerebellar
infarction in young patients. Stroke 1997; 28: 2400-2404.
2. Hinse P, Thie A, Lachenmayer L. Dissection of the extracranial vertebral
artery:
report of four cases and review of the literature. J Neurol Neurosurg
Psychiatry
1991; 54: 863-869.
3. Capian LR, Baquis GD, Pessin MS, et al. Dissection of the intracranial
vertebral
artery. Neurology 1988; 38: 868-877.
4. Lagone J. Chiropractors: a consumer guide. Massachusetts: Addison-Wesley
Pub
lishing Company, 1982; 80, 123.
5. Nakamura CT, Lau JM, Polk N, Popper JS. Vertebral artery dissection
caused by
chiropractic manipulation. J Vase Surg 1991; 14: 122-124.
6. Tatlow WIFT, Barnmer HG. Syndrome of vertebral artery compression.
Neurology
1940; 7: 331-340.
7. Rogers v Whittaker(1991) 23 NSW LR 600; [19921175 CLR 479. Q
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